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Flat bands have empowered novel phenomena such as robust canalization with strong localization, high-collimation and low-loss propagation. However, the spatial symmetry protection in photonic or acoustic lattices naturally forces flat bands to manifest in pairs aligned at an inherently specific angle, resulting in a fixed bidirectional canalization. Here, we report an acoustic flat-band metasurface, allowing not only unidirectional canalization at all in-plane angles but also robust tunability in band alignment. The twist, tilt, and skew angles of the bilayer metasurface can be flexibly controlled to break both in-plane and out-of-plane spatial symmetries. These features can thereby turn arbitrary twist angles between bilayers into ‘magic angles’, while maintaining all unidirectional canalization and band alignment tunability. This work may significantly contribute to pushing twisted moiré physics into higher dimensions and facilitate the application of advanced acoustic or optical devices. Flat bands have empowered novel phenomena such as canalization, high-collimation and low-loss propagation. Here, the authors propose the concept of symmetry broken moiré systems, which overcomes the limitations of fixed flat bands, enabling multiple and unidirectional canalizations.

Moiré quasicrystals, formed by stacking periodic structures with a relative twist between them, exhibit many exotic phenomena. Their quasiperiodicity leads to effects such as light localization-delocalization transitions, superconductivity, topological states, and quasiband dispersion. However, weak interlayer interactions, the scalar nature of acoustic fields, and longer wavelengths severely limit the demonstration of these phenomena in acoustics. Here, we report an acoustic moiré quasicrystal that not only achieves a localization-delocalization transition, but also enables wave propagation shifting from diffusion to canalization or localization as a function of the quasicrystal geometry. Unlike conventional two-dimensional materials, the designed sublattice provides tailorable anisotropy and spatial broken symmetry, allowing quasicrystal structures to exhibit reconfigurable nontrivial dispersion. Furthermore, by introducing a uniform tilt angle in the unit cells breaks the spatial symmetry of the moiré quasicrystal, resulting in partial attenuation and disappearance of the wave within the localization pattern. Our findings pave a new avenue for controlling the properties of acoustic wave patterns, and benefit potential applications in energy transfer, subwavelength wave propagation, and highly sensitive sensors. Moiré quasicrystals exhibit many exotic phenomena. Here, the authors report an acoustic moiré quasicrystal that not only achieves a localization-delocalization transition, but also enables wave propagation shifting from diffusion to canalization or localization.

Prostate cancer (PCa) is an age-associated malignancy with high morbidity and mortality rate, posing a severe threat to public health. Cellular senescence, a specialized cell cycle arrest form, results in the secretion of various inflammatory mediators. In recent studies, senescence has shown an essential role in tumorigenesis and tumor development, yet the extensive effects of senescence in PCa have not been systematically investigated. Here, we aimed to develop a feasible senescence-associated prognosis model for early identification and appropriate management in patients with PCa. The RNA sequence results and clinical information available from The Cancer Genome Atlas (TCGA) and a list of experimentally validated senescence-related genes (SRGs) from the CellAge database were first obtained. Then, a senescence-risk signature related with prognosis was constructed using univariate Cox and LASSO regression analysis. We calculated the risk score of each patient and divided them into high-risk and low-risk groups in terms of the median value. Furthermore, two datasets (GSE70770 and GSE46602) were used to assess the effects of the risk model. A nomogram was built by integrating the risk score and clinical characteristics, which was further verified using ROC curves and calibrations. Finally, we compared the differences in the tumor microenvironment (TME) landscape, drug susceptibility, and the functional enrichment among the different risk groups. We established a unique prognostic signature in PCa patients based on eight SRGs, including CENPA, ADCK5, FOXM1, TFAP4, MAPK, LGALS3, BAG3, and NOX4, and validated well prognosis-predictive power in independent datasets. The risk model was associated with age and TNM staging, and the calibration chart presented a high consistency in nomogram prediction. Additionally, the prognostic signature could serve as an independent prediction factor due to its high accuracy. Notably, we found that the risk score was positively associated with tumor mutation burden (TMB) and immune checkpoint, whereas negatively correlated with tumor immune dysfunction and exclusion (TIDE), suggesting that these patients with risk scores were more sensitive to immunotherapy. Drug susceptibility analysis revealed differences in the responses to general drugs (docetaxel, cyclophosphamide, 5-Fluorouracil, cisplatin, paclitaxel, and vincristine) were yielded between the two risk groups. Identifying the SRG-score signature may become a promising method for predicting the prognosis of patients with PCa and tailoring appropriate treatment strategies.

Background Castration-resistant prostate cancer (CRPC) has been a major cause of tumor-associated death among men worldwide. The discovery of novel therapeutic medicines for CRPC remains imperative. Atractylenolide I (ATR-I), a prominent bioactive component from Atractylodes macrocephala, exhibits powerful anticancer potentials in various malignancies. Nevertheless, the ATR-I’s activity on CRPC has not been reported. Methods An enzalutamide-resistant (EnzR) cell line was successfully constructed. CCK-8, EdU, wound healing, Transwell assays, flow cytometry, and xenograft tumor models were applied to investigate the antitumor activity of ATR-I against CRPC. The changes in the gene expression profiles after ATR-I treatment were analyzed using RNA sequencing. Results ATR-I suppressed the proliferative and migratory abilities of AR + and AR − CRPC cells, while triggering cell cycle arrest and apoptosis. ATR-I also exerted anti-cancer activity on EnzR cell lines. Intriguingly, a combination of ATR-I with enzalutamide synergistically induced more apoptosis of tumor cells. RNA-sequencing identified kinesin family member 15 (KIF15) as a potential target of ATR-I. KIF15 was up-regulated in prostate cancer (PCa), and its higher level was associated with poorer clinical outcomes. Further investigation showed that ATR-I mediated ubiquitin-proteasomal degradation of AR/AR-V7 through targeting KIF15, resulting in CRPC repression. Finally, our in vivo experiment verified that ATR-I alone or in combination with enzalutamide retarded the growth of EnzR xenograft tumors. Conclusions These findings identified ATR-I as a promising therapeutic drug for overcoming enzalutamide resistance in CRPC patients and increased our understanding about its antitumor mechanisms. Graphical abstract

In the realm of ballistic target analysis, micro-motion attributes, such as warhead precession, nutation, and decoy oscillations, play a pivotal role. This paper addresses these critical aspects by introducing an advanced analytical model for assessing the Doppler power spectra of convex quadric revolution bodies during precession. Our model is instrumental in calculating the Doppler shifts pertinent to both precession and swing cones. Additionally, it extends to delineate the Doppler power spectra for configurations involving cones and sphere–cone combinations. A key aspect of our study is the exploration of the effects exerted by geometric parameters and observation angles on the Doppler spectra, offering a comparative perspective of various micro-motion forms. The simulations distinctly demonstrate how different micro-motion patterns of a cone influence the Doppler power spectra and underscore the significance of geometric parameters and observational angles in shaping these spectra. This research not only contributes to enhancing LIDAR target identification methodologies but also lays a groundwork for future explorations into complex micro-motions like nutation.

Objective. This study is aimed at using genes related to the peroxisome proliferator-activated receptor (PPAR) pathway to establish a prognostic risk model in kidney renal clear cell carcinoma (KIRC). Methods. For this study, we first found the PPAR pathway-related genes on the gene set enrichment analysis (GSEA) website and found the KIRC mRNA expression data and clinical data through TCGA database. Subsequently, we used R language and multiple R language expansion packages to analyze the expression, hazard ratio analysis, and coexpression analysis of PPAR pathway-related genes in KIRC. Afterward, using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) website, we established the protein-protein interaction (PPI) network of genes related to the PPAR pathway. After that, we used LASSO regression curve analysis to establish a prognostic survival model in KIRC. Finally, based on the model, we conducted correlation analysis of the clinicopathological characteristics, univariate analysis, and multivariate analysis. Results. We found that most of the genes related to the PPAR pathway had different degrees of expression differences in KIRC. Among them, the high expression of 27 genes is related to low survival rate of KIRC patients, and the high expression of 13 other genes is related to their high survival rate. Most importantly, we used 13 of these genes successfully to establish a risk model that could accurately predict patients’ prognosis. There is a clear correlation between this model and metastasis, tumor, stage, grade, and fustat. Conclusions. To the best of our knowledge, this is the first study to analyze the entire PPAR pathway in KIRC in detail and successfully establish a risk model for patient prognosis. We believe that our research can provide valuable data for future researchers and clinicians.

Androgen deprivation therapy (ADT) remains the standard treatment for advanced prostate cancer (PCa); however, most patients ultimately progress to lethal castration-resistant PCa (CRPC). Emerging evidence implicates RNA N⁶-methyladenosine (m⁶A) modification as a key regulator of cancer biology, yet its role in CRPC remains poorly understood. As a critical adaptor in the m⁶A methyltransferase complex, RNA-binding motif protein 15 (RBM15) directs m⁶A deposition to specific mRNA targets. Here, we identified RBM15 as the key methyltransferase member significantly upregulated in CRPC tissues and strongly correlated with poor patient survival. Functionally, RBM15 overexpression reduces PCa cell sensitivity to enzalutamide, whereas its knockdown suppresses tumor growth and invasion. Mechanistically, RBM15 is an androgen-responsive protein whose expression increases upon chronic androgen deprivation. It catalyzes m⁶A methylation at position A1384 of damaged DNA binding protein 1 ( DDB1 ) mRNA, leading to YTHDF2-dependent transcript decay and reduced DDB1 protein levels. Lower DDB1 impairs K48-linked polyubiquitination of the androgen receptor (AR), thereby stabilizing AR and amplifying AR signaling. Importantly, AR transcriptionally activates RBM15 , forming a feed-forward loop that drives CRPC progression. Collectively, our findings establish RBM15 as a central epitranscriptomic driver of CRPC and identify the RBM15–DDB1–AR axis as a promising therapeutic target. Dual inhibition of RBM15 and AR may offer a novel strategy to overcome treatment resistance in advanced PCa.

Actuator faults and external disturbances, which are inevitable due to material fatigue, operational wear and tear, and unforeseen environmental impacts, cause significant threats to the control reliability and performance of networked systems. Therefore, this paper primarily focuses on the distributed adaptive bipartite consensus tracking control problem of networked Euler–Lagrange systems (ELSs) subject to actuator faults and external disturbances. A robust distributed control scheme is developed by combining the adaptive distributed observer and neural-network-based tracking controller. On the one hand, a new positive definite diagonal matrix associated with an asymmetric Laplacian matrix is constructed in the distributed observer, which can be used to estimate the leader’s information. On the other hand, neural networks are adopted to approximate the lumped uncertainties composed of unknown matrices and external disturbances in the follower model. The adaptive update laws are designed for the unknown parameters in neural networks and the actuator fault factors to ensure the boundedness of estimation errors. Finally, the proposed control scheme’s effectiveness is validated through numerical simulations using two types of typical ELS models: two-link robot manipulators and quadrotor drones. The simulation results demonstrate the robustness and reliability of the proposed control approach in the presence of actuator faults and external disturbances.

Ribophorin II (RPN2) is a highly conserved glycoprotein involved in the N-linked glycosylation of multiple proteins. RPN2 was reported to be associated with malignant phenotype in several tumors. However, the function of RPN2 in bladder cancer (BCa) remains unclear. Expression of RPN2 in BCa and adjacent tissues was compared by bioinformatics analysis, immunohistochemistry, and Western blotting. qRT-PCR was performed to explore the correlation between RPN2 expression and various clinical features in 38 patients. We assessed the effects of RPN2 on the biological activity of BCa both in vitro and in vivo, and explored its potential mechanisms based on gene set enrichment analysis (GSEA). We found that RPN2 was highly expressed in human BCa compared with normal adjacent tissues. There was a significant positive correlation between higher RPN2 mRNA levels and tumor T stage, lymph node (LN) metastasis and the degree of pathological differentiation in 38 patients with BCa. We further demonstrated that RPN2 silencing inhibited the growth and metastasis of BCa both in vitro and in vivo. Western blotting revealed that RPN2 knockdown suppressed epithelial-mesenchymal transition (EMT) and inhibited the PI3K-Akt pathway. These data suggest that RPN2 functions as an oncogene to promote tumor development and is a promising prognostic factor and therapeutic target in BCa.

Purpose: To explore the effects of immunotherapy and tumour treatment on patients with GABABR encephalitis, evaluate the correlation between immune cell subsets and disease activity, and investigate effective prognostic factors. Patients and Methods: Twenty patients with γ-aminobutyric acid B receptor (GABABR) encephalitis were enrolled from December 2015 to April 2020. The clinical data, modified Rankin Scale (mRS) score, prognosis and percentage of serum lymphocytes were recorded. Results: All patients received first-line immunotherapy. The median mRS scores were 4 and 3 before and after first-line immunotherapy (P< 0.01). Seven patients received second-line immunotherapy and had median mRS scores of 3 and 2 before and after second-line immunotherapy (P=0.015). Small-cell lung cancer was detected in twelve patients. Among the patients who died because of tumours, patients who received tumour treatment lived longer than patients who did not receive tumour treatment (P=0.025). All four surviving patients who received tumour treatment had good outcomes (mRS≤ 2). The median serum CD19+B cell percentage in sixteen patients were 20.00% and 13.42% prior first-line immunotherapy and at the last follow-up (P< 0.01). After a maximum follow-up of 54 months (median: 12; range: 3– 54), eleven patients (55%) had a poor prognosis (mRS> 2). Predictors of a poor prognosis were older age (P=0.031), delayed initial improvement after immunotherapy (> 4 weeks) (P=0.038) and respiratory failure (P=0.038). Conclusion: Aggressive immunotherapy and tumour treatment contribute to improvements in neurological function and a better prognosis of patients with GABABR encephalitis. The serum CD19+B cell percentage may be an indicator of disease activity. Older age, delayed initial improvement after immunotherapy, and respiratory failure may be associated with poor outcomes.